scholarly journals Cardiac complications during the active phase of COVID-19: review of the current evidence

Author(s):  
Mohammad Said Ramadan ◽  
◽  
Lorenzo Bertolino ◽  
Tommaso Marrazzo ◽  
Maria Teresa Florio ◽  
...  

AbstractGrowing reports since the beginning of the pandemic and till date describe increased rates of cardiac complications (CC) in the active phase of coronavirus disease 2019 (COVID-19). CC commonly observed include myocarditis/myocardial injury, arrhythmias and heart failure, with an incidence reaching about a quarter of hospitalized patients in some reports. The increased incidence of CC raise questions about the possible heightened susceptibility of patients with cardiac disease to develop severe COVID-19, and whether the virus itself is involved in the pathogenesis of CC. The wide array of CC seems to stem from multiple mechanisms, including the ability of the virus to directly enter cardiomyocytes, and to indirectly damage the heart through systemic hyperinflammatory and hypercoagulable states, endothelial injury of the coronary arteries and hypoxemia. The induced CC seem to dramatically impact the prognosis of COVID-19, with some studies suggesting over 50% mortality rates with myocardial damage, up from ~ 5% overall mortality of COVID-19 alone. Thus, it is particularly important to investigate the relation between COVID-19 and heart disease, given the major effect on morbidity and mortality, aiming at early detection and improving patient care and outcomes. In this article, we review the growing body of published data on the topic to provide the reader with a comprehensive and robust description of the available evidence and its implication for clinical practice.

2020 ◽  
Vol 9 (3) ◽  
pp. 59-68
Author(s):  
S. S. Murashko ◽  
I. N. Pasechnik ◽  
S. A. Berns

A new concept was adopted by the Fourth Universal Definition of MI Expert Consensus Document in 2018 – periprocedural myocardial injury after cardiac- and noncardiac interventions, which is distinct from myocardial infarction.It is difficult to diagnose a heart attack and myocardial damage after noncardiac surgery.Postoperative myocardial injury increases mortality and worsens the long-term prognosis and quality of treatment.The quality of surgical care is determined by surgical techniques and the course of the postoperative period. Although complications often negate the results of brilliantly performed surgery, many of them would happen irrespective of surgeon`s actions. The development of complications determining the outcome of treatment can be associated with cardiac pathology. Cardiac complications may develop due to existing comorbidities, hemodynamic instability during surgery, cardiotoxic effect of drugs, etc. In 40% of cases, the risk of cardiac death after noncardiac surgery is associated with the development of perioperative myocardial infarction or myocardial injury. Myocardial infarction is the most demonstrative complication, although it is difficult to diagnose in the perioperative period in case of asymptomatic course. The link between postoperative myocardial infarction and lethality is beyond doubt. Adopted in 2018, the Fourth Universal Definition of MI Expert Consensus Document introduced a new concept of periprocedural myocardial injury after cardiac- and noncardiac interventions, which are distinct from myocardial infarction. Myocardial injury requires laboratory tests to be diagnosed. However, myocardial injury itself affects postoperative mortality and significantly worsens the long-term prognosis and quality of treatment. This article reports the features of the etiopathogenetic mechanisms of cardiac complications during surgical care, as well as the multifactorial genesis of myocardial injury. The analysis of modern scientific literature on the diagnosis of myocardial damage is given. The need for early diagnosis of myocardial damage to create optimal management tactics for patients undergoing noncardiac interventions is demonstrated.


2020 ◽  
Vol 5 (5) ◽  
pp. 158-163
Author(s):  
V. I. Lysenko ◽  
◽  
E. A. Karpenko ◽  
Ya. V. Morozova

The study of intraoperative fluid therapy tactics has been of great interest over the past few years, especially in people with concomitant coronary heart disease, as they make up a significant proportion of all surgical patients. The purpose of our study was to assess the risk of intraoperative myocardial damage in patients with concomitant coronary heart disease depending on the fluid regimen used based on monitoring of hemodynamic parameters, electrocardiogram and biomarkers of myocardial damage. Material and methods. The study involved 89 patients, who were divided into two groups depending on the tactics of intraoperative fluid therapy – restrictive and liberal. In order to detect cardiac complications at different stages, we assessed biomarkers of myocardial damage Troponin I, NT-proBNP by solid-phase enzyme-linked immunosorbent assay (ELISA). Results and discussion. Analysis of the obtained data showed that MINS (myocardial injury in noncardiac surgery) incidents were diagnosed in 5 patients (11.1%) in the first group and in 6 patients (13.6%) in the second. In patients of both groups there was an increase in NT-proBNP in the dynamics at all stages, and in the 2nd group, with a liberal regimen of intraoperative fluid therapy, it was more pronounced. It should be noted that the obtained values of NT-proBNP in all patients did not differ significantly from those allowed for this age group; such dynamics of NT-proBNP may indicate a relative risk of complications of liberal fluid therapy in patients with baseline heart failure. One of the important points when choosing the mode of fluid therapy in patients with high cardiac risk is the assessment of the initial volemic status and careful monitoring of water balance in the perioperative period with the desire for "zero" balance. The obtained dynamics of laboratory markers of myocardial damage indicates that in patients with a significant reduction in cardiac reserves compensated for heart failure, a restrictive fluid regimen is preferable, which is also confirmed by slight changes in the concentration of biomarkers. Conclusion. Thus, the study demonstrated the relative safety of selected fluid regimens in patients with concomitant coronary heart disease without signs of congestive heart failure


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
F.A.M Cardozo ◽  
T Artioli ◽  
B Caramelli ◽  
D Calderaro ◽  
P.C Yu ◽  
...  

Abstract Introduction Patients submitted to arterial vascular surgeries are at a high risk of postoperative cardiac and non-cardiac complications, therefore developing strategies to lower perioperative complications is essential to optimize outcomes for this subgroup. Recent studies have suggested that the period of the day in which surgeries are performed may influence postoperative major cardiovascular complications but there is still no evidence of this association in vascular surgeries. Purpose Our goal is to evaluate whether the period of the day in which surgeries are performed may influence mortality and cardiovascular outcomes in patients undergoing non-cardiac vascular procedures. Methods Patients who underwent non-cardiac vascular surgeries between 2012 and 2018 were prospectively included at our cohort. For this analysis, subjects were categorized into two groups: those who underwent surgery in the morning (7am - 12am) and those who underwent surgery in the afternoon/night (12:01pm - 6:59am). The primary endpoints were to compare the incidence of major adverse cardiac events (MACE - acute myocardial infarction, acute heart failure, arrhythmias, and cardiovascular death) and total mortality between morning and afternoon/night surgeries within 30 days and one year. The secondary endpoint was the incidence of perioperative myocardial injury (PMI) in both groups. PMI was defined as an absolute elevation of high-sensitivity cardiac troponin T (hs-cTnT) concentrations ≥14ng/L. Multivariable analysis using Cox proportional regression (with Hazard Ratio – HR and Confidence Interval – 95% CI) was performed to adjust for confounding variables, including emergency and urgent surgeries. Results Of 1267 patients included, 1002 (79.1%) underwent vascular surgery in the morning and 265 (20.9%) in the afternoon/night. After adjusting for confounding variables, the incidence of MACE at 30 days was higher among those who underwent surgery in the afternoon/night period (37.4% vs 20.4% – HR 1.43, 95% CI: 1.10–1.85; p=0.008). Mortality rates were also elevated in the afternoon/night group (21.5% vs 9.9%, HR 1.59, 95% CI: 1.10–2.29; p=0.013). After one-year of follow-up the worst outcomes persisted in patients operated in the afternoon/night: higher incidence of MACE (37.7% vs 21.2%, HR 1.37, 95% CI: 1.06–1.78; p=0.017) and mortality (35.8% vs 17.6%, HR 1.72, 95% CI 1.31–2.27; p<0.001). There was no significant difference in the incidence of PMI between groups (p=0.8). Conclusions In this group of patients, being operated in the afternoon/night period was independently associated with increased mortality rates and incidence of MACE. Mortality and MACE at one year Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): FAPESP - Fundação de Amparo a Pesquisa do Estado de São Paulo


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hao Chen ◽  
Hiromi Matsumoto ◽  
Nobuyuki Horita ◽  
Yu Hara ◽  
Nobuaki Kobayashi ◽  
...  

AbstractRisk factors associated with mortality in invasive pneumococcal disease remain unclear. The present work is a meta-analysis of studies that enrolled only patients with invasive pneumococcal disease and reported on mortality. Potentially eligible reports were identified from PubMed, CHAHL, and Web of Science, comprising 26 reports in total. Overall mortality for invasive pneumococcal disease was reported as 20.8% (95% confidence interval (CI) 17.5–24%). Factors associated with mortality were age (odds ratio (OR) 3.04, 95% CI 2.5–3.68), nursing home (OR 1.62, 95% CI 1.13–2.32), nosocomial infection (OR 2.10, 95% CI 1.52–2.89), septic shock (OR 13.35, 95% CI 4.54–39.31), underlying chronic diseases (OR 2.34, 95% CI 1.78–3.09), solid organ tumor (OR 5.34, 95% CI 2.07–13.74), immunosuppressed status (OR 1.67, 95% CI 1.31–2.14), and alcohol abuse (OR 3.14, 95% CI 2.13–4.64). Mortality rates with invasive pneumococcal disease remained high, and these findings may help clinicians provide appropriate initial treatment for this disease.


Author(s):  
Kang Zhou ◽  
Yan Xu ◽  
Qiong Wang ◽  
Lini Dong

Abstract Myocardial injury is still a serious condition damaging the public health. Clinically, myocardial injury often leads to cardiac dysfunction and, in severe cases, death. Reperfusion of the ischemic myocardial tissues can minimize acute myocardial infarction (AMI)-induced damage. MicroRNAs are commonly recognized in diverse diseases and are often involved in the development of myocardial ischemia/reperfusion injury. However, the role of miR-431 remains unclear in myocardial injury. In this study, we investigated the underlying mechanisms of miR-431 in the cell apoptosis and autophagy of human cardiomyocytes in hypoxia/reoxygenation (H/R). H/R treatment reduced cell viability, promoted cell apoptotic rate, and down-regulated the expression of miR-431 in human cardiomyocytes. The down-regulation of miR-431 by its inhibitor reduced cell viability and induced cell apoptosis in the human cardiomyocytes. Moreover, miR-431 down-regulated the expression of autophagy-related 3 (ATG3) via targeting the 3ʹ-untranslated region of ATG3. Up-regulated expression of ATG3 by pcDNA3.1-ATG3 reversed the protective role of the overexpression of miR-431 on cell viability and cell apoptosis in H/R-treated human cardiomyocytes. More importantly, H/R treatments promoted autophagy in the human cardiomyocytes, and this effect was greatly alleviated via miR-431-mimic transfection. Our results suggested that miR-431 overexpression attenuated the H/R-induced myocardial damage at least partly through regulating the expression of ATG3.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jose A Barrabes ◽  
Javier Inserte ◽  
Maribel Mirabet ◽  
Adoracion Quiroga ◽  
Victor Hernando ◽  
...  

Objective: Platelets activated during experimental acute myocardial infarction (AMI) contribute to myocardial injury. We aimed to investigate whether platelets from patients with AMI increase myocardial damage after transient ischemia in isolated rat hearts and the modification of this effect by the P2Y 12 receptor antagonist cangrelor and the GPIIb/IIIa receptor blocker abciximab. Methods: Platelets were obtained from 9 AMI patients (7 thrombolyzed, all on aspirin) within 24 h after symptom onset. Incubation with 100 μM cangrelor or 50 μg/ml abciximab resulted, respectively, in 78 ± 4 and 90 ± 2% inhibition of aggregation (optical aggregometry). Isolated rat hearts (four simultaneous experiments per patient) were subjected to 40 min of global ischemia and 60 min of reperfusion. Hearts received no additional intervention (Control) or were infused during the 5 min prior to ischemia with platelets (22.5x10 6 /min), either untreated or treated with cangrelor or abciximab. Results: P-selectin expression (flow cytometry) in isolated platelets before infusion was 31 ± 3% (P = NS between groups). Platelets augmented myocardial injury, as demonstrated by worse left ventricular developed pressure (LVDevP), higher left ventricular enddiastolic pressure (LVEDP) and coronary resistance, and greater LDH release and infarct size (TTC staining), and both cangrelor and abciximab greatly attenuated these effects (Table ). Conclusions: Activated platelets from patients with AMI increase myocardial injury after ischemia and reperfusion, and cangrelor and abciximab attenuate this effect. The results support the notion that very early antiplatelet treatment may increase myocardial salvage by direct effects on the microcirculation in these patients.


2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Pei-Ling I Hsu ◽  
Fan-E Mo

Introduction: Matricellular protein CCN1 is expressed in myocardial infarction, pressure overload, and ischemia in mice, and in patients with a failing heart. Despite its well-documented angiogenic activities, CCN1 promotes fibroblast apoptosis in some contexts. The role of CCN1 in an injured heart was not clear. We assessed the hypothesis that CCN1 plays a detrimental role and mediates cardiac injury through its proapoptotic activities. Methods and Results: To test the role of CCN1 in cardiac injury, we employed two different myocardial injury models in mice, including a work-overload-induced injury created by isoproterenol treatment (ISO; 100 mg/kg/day; s.c. for 5 days; n= 6 for each group) and an injury induced by the cardiotoxicity of doxorubicin (DOX, single dose of 15 mg/kg; i.p. sacrificed after 14 days). Ccn1 expression was induced in the damaged myocardium in both injury models. A line of knock-in mice carrying an apoptosis-defective Ccn1 mutant allele, Ccn1-dm , which has disrupted integrin α 6 β 1 binding sites, were tested in the ISO- or DOX -induced cardiac injury. Myocardial damage was seen in tissues from wile-type (WT) hearts after receiving ISO. Ccn1 dm/dm (DM) mice possessed remarkable resistance against ISO or DOX treatments and exhibited no tissue damage or fibrosis compared to WT mice after H&E or Masson’s trichrome stainings. DM mice were resistant to both ISO- and DOX-induced cardiac cell apoptosis, indicating that CCN1 is critically mediating cardiomyocyte apoptotic death in cardiac injury. Moreover, we found that death factor Fas ligand (FasL) and its receptor Fas were upregulated in WT mice receiving ISO or DOX treatments by immunohistochemical staining, compared with the PBS-control. 8-OHdG-positive, a marker for oxidative stress, cardiomyocytes were increased by ISO or DOX treatments as well. In contrast, the expression of Fas/FasL, and the 8-OHdG-positive cardiomyocytes in the myocardium of DM mice were not changed by ISO or DOX. Conclusions: We identify CCN1 as a novel pathophysiological regulator of cardiomyocyte apoptosis in cardiac injury. Blocking apoptotic function of CCN1 effectively prevents myocardial injury in mice. CCN1 and its receptor α 6 β 1 represent promising future therapeutic targets in cardiac injury.


2020 ◽  
pp. 1-3
Author(s):  
Hasan Ibrahim Al-Balas ◽  

Introduction: Coronavirus disease 2019 (COVID-19) is an emerging global health care threat that is caused by a novel coronavirus named 2019-nCoV (SARS-CoV-2). The first case of diagnosed COVID-19 patient was declared in Jordan in early March 2020. As of June 8, Jordan had confirmed 831 cases, with 9 deaths, with an overall mortality rate of 1.08%. As there is no published data about critically ill patients in Jordan, we aimed to describe the characteristics and outcomes of critically ill COVID-19 patients in a tertiary hospital in Jordan.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Ivo A van der Bilt ◽  
Djo Hasan ◽  
W. P Vandertop ◽  
Arthur A Wilde ◽  
Ale Algra ◽  
...  

Cardiac complications after subarachnoid hemorrhage (SAH) occur frequently, but their prognostic significance remains unclear. We performed a meta-analysis to assess whether echocardiographic wall motion abnormalities (WMA), electrocardiographic (ECG) changes, or elevated markers for myocardial damage are related to the occurrence of delayed cerebral ischemia (DCI) or death. Methods All articles that reported on cardiac abnormalities after aneurysmal SAH, that met predefined criteria, and were published between 1960 and 2007 were assessed. Data were extracted on predefined methodological criteria, patient characteristics, prevalence of cardiac abnormalities, and DCI or death. We calculated pooled relative risks (RR) with corresponding 95% confidence intervals (CI) for the separate cardiac abnormalities and outcome. Results We included 25 studies (16 prospective), comprising 2690 patients (mean age 53 years; 35% was male). The figure shows the univariable RRs of the determinants for death. For DCI we found a significant association with WMA (RR 2.10 [CI 1.17, 3.78]); Troponin RR 3.15 [CI 2.27, 4.38]; CK-MB RR: 2.90 [CI 1.86, 4.52]; BNP RR: 4.52 [CI 1.79, 11.39]; and ST depression RR: 2.40 [CI 1.2, 4.9]. No significant associations were found for DCI and ST elevation RR: 2.1 [CI 0.7, 5.7]; T wave abnormality RR: 0.9 [CI 0.5, 1.7]; U wave RR: 0.7 [CI 0.4, 1.3] or prolonged QT RR: 1.0 [CI 0.5, 2.3]. Conclusion Cardiac abnormalities increase the risk of DCI and death after SAH. Future research should be directed towards elucidating the multivariable relationship between the cardiac prognosticators, the pathophysiological mechanism and potential treatment options.


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